The paper presents the theoretical considerations on the role of endocrine and metabolic alterations accompanying COVID-19 infection. These alterations may be presumed on the basis of the following two observations. Firstly, the virus SARS-CoV-2 responsible for the COVID-19 infection uses an important renin-angiotensin system (RAS) element - angiotensin-converting enzyme 2 (ACE2) - as a receptor protein for entry into target cells and, in consequence, disturbs the function of the main (circulating) renin-angiotensin-aldosterone system (RAAS) and of the local renin-angiotensin system localized in different tissues and organs. The binding of SARS-CoV-2 to ACE2 leads to the downregulation of this enzyme and, in the aftermath, to the excess of angiotensin II and aldosterone. Thus, in the later stage of COVID-19 infection, the beneficial effects of ACEI and ARB could be presumed. It is hypothesized that the local RAS dysregulation in the adipose tissue is the main cause of the negative role of obesity as a risk factor of severe outcome of the COVID-19 infection. Secondly, the outcome of COVID-19 strongly depends on the age of the patient. Age-related hormonal deficiencies, especially those of melatonin and dehydroepiandrosterone, may contribute to morbidity/mortality in older people. The usefulness of melatonin and angiotensin converting enzyme inhibitors/angiotensin receptor 1 blockers (the latter only in later phases of the infection) as adjuvant drugs is probable but needs thorough clinical trials.